Molecular events involved in neuronal death induced in the mouse hippocampus by in-vivo injection of kainic acid
Molecular events involved in neuronal death induced in the mouse hippocampus by in-vivo injection of kainic acid
复制标题
DOI：
10.1016/s0169-328x(01)00197-8
复制
发表时间：
2001-09-30
期刊：
影响因子：
--
通讯作者：
Rondouin, G
中科院分区：
文献类型：
--
作者：
Djebaïli, M;Lerner-Natoli, M;Rondouin, G
细胞凋亡是由涉及几种机制的程序性细胞级联激活引起的。在本研究中，我们已经调查了这个级联的三个分子，p53，Bax和caspase-3，在海人酸（KA）管理诱导的小鼠海马神经元死亡的含义。利用免疫细胞化学、蛋白质印迹和酶活性定量，我们在p53+/+和p53-/-动物中观察到KA通过p53依赖性和非依赖性途径诱导神经元死亡。此外，神经毒性损伤后细胞凋亡（TUNEL标记）和bax和caspase-3蛋白表达的增加似乎明显依赖于p53的表达。(C)2001 Elsevier Science B V.保留所有权利。
Apoptosis results from the activation of a programmed cellular cascade involving several mechanisms. In the present study, we have investigated the implication of three molecules of this cascade, p53, Bax and caspase-3, in neuronal death induced by kainic acid (KA) administration in mouse hippocampus. Using immunocytochemistry, western blot and quantification of enzyme activity, we observed in p53+/+ and p53-/- animals that KA induced neuronal death by both p53-dependent and independent pathways. Moreover, apoptosis (labeled by TUNEL) and the increase of bax and caspase-3 protein expression after the neurotoxic insult appeared to clearly depend on p53 expression. (C) 2001 Elsevier Science B V. All rights reserved.